Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease

Figure 2

Mechanism of 5-HT in the mouse pancreatic beta-cells during pregnancy. In pregnant mice, prolactin (PRL) stimulates islet prolactin receptors (PRLRs) to trigger a strong upregulation of both isoforms of TPH. TPH upregulation activates 5-HT synthesis in some pancreatic β-cells, which in turn induce GSIS. The insulin secretion is upregulated by the 5-HT_2B receptor (5-HT_2BR) and downregulated by the 5-HT_1D receptor (5-HT_1DR) in β-cells, making 5-HT a paracrine regulator of β-cell proliferation. 5-HT_3AR channels in wild-type animals allow a 5-HT-mediated influx of cations, depolarizing the resting membrane potential and lowering the threshold for glucose-induced insulin exocytosis.